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Children's exposure to Di(2-ethylhexyl)phthalate and dibutylphthalate plasticizers from school meals.

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Published: September 06, 2011

pubs.acs.org/JAFC

Children’s Exposure to Di(2-ethylhexyl)phthalate and

Dibutylphthalate Plasticizers from School Meals

Teresa Cirillo,*

,†

Evelina Fasano,

Enrica Castaldi,

Paolo Montuori,

and Renata Amodio Cocchieri

Department of Food Science, University of Naples“Federico II”, Via Universita 100, 80055 Portici, Naples, ItalyDepartment of Preventive Medical Sciences, University of Naples“Federico II”, Via Sergio Pansini 5, 80131 Naples, Italy

ABSTRACT:Packed school meals for children 3 10 years old were studied to evaluate the levels of di(2-ethylhexyl)phthalate (DEHP) and di-n-butylphthalate (DBP) and the influence of the packaging process on meal contamination, and their contribution to daily intake was estimated. The packaging consisted of polyethylene-coated aluminum (PE/Al) dishes thermally welded by a polyethyleneterephthalate-coated aluminum (PET/Al) foil. Foodstuffs before processing were analyzed, too. Total meals before packaging and after packaging were collected. It was found that 92% of foodstuffs employed in meal preparation contained DEHP, and 76% of them DBP, at detectable levels. In cooked foods before packaging the DEHP median concentration levels varied from 111.4 to 154.8 ng/g ww and those of DBP between 32.5 and 59.5 ng/g ww. In packed meals the DEHP median values ranged from 127.0 to 253.3 ng/g ww, and DBP median values varied from 44.1 to 80.5 ng/g ww. The mean increases of median concentrations of DEHP in cooked foods before and after packaging were 113 and 125% for DBP. For nursery and primary school children DEHP intake via school meals can raise on average the respective EFSA TDI by 18 and 12% and that of DBP by 50 and 30%.

KEYWORDS:di(2-ethylhexyl)phthalate, dibutylphthalate, packed school meals, children's exposure ’ INTRODUCTION

Children are particularly susceptible and vulnerable to xeno-biotics for different metabolic and physiological activities that rotate during the life cycle. The specific vulnerability of childhood is incidental to many intrinsic or expressed factors of children, such as greater pulmonary air volume, more permeable skin, and larger amounts of food and water ingested in relation to body weight, which is why exposure from respiration, through the skin, and via food is higher than in adults. Furthermore, children spend a considerable time indoors, such as at home, in a day nursery, and in school, where dust can represent a major source of exposure to xenobiotics;1,2ground contact, the habit of sucking and playing with pets treated with insecticides, and inadequate hand-washing can further increase children’s chemical intake. Furthermore, with regard to food, as children typically consume milk, dairy products, and baby foods, the pollutants they ingest may be very different from those of adults.

In industrialized countries, exposure to some xenobiotics is considered to be probably involved in an increase of disorders in the immune system, neurobehavior, and puberty. Many ubiquitous pollutants such as polychlorinated and polybrominated biphenyls (PCBs, PBBs), dioxins, some biocides and metals, and, principally, phthalates (PAEs) are considered to be potentially involved in endocrine system interference and disruption. PAEs are synthetic organic chemicals introduced in the 1920s, among which, for their use as plasticizers in resins and polymers such as PVC, the main compounds are di(2-ethylhexyl)phthalate (DEHP) and di-n-butylphthalate (DBP).3 4 PAE toxicological studies have shown negative effects on the development of the male repro-ductive system in rodents5,6 and possibly in humans.7 Such findings are thought to be due to the endocrine disruptive action of phthalates during the phase of sexual differentiation in the fetus.8 DEHP and DBP and their metabolites have especially been shown to cause antiandrogenic effects manifested as decreased anogenital

distance (AGD), cryptorchidism, decreased testosterone levels, and sperm production and infertility. According to the European Union (EU) criteria for classification and labeling of dangerous substances, DEHP has been classified in category 2 as toxic both for reproduction and for development (R60-61).9Recently Kim et al.,10 on the basis of the results of a study on 261 Korean children, aged 8 11 years, on the relationship between the clinical syndrome of attention-deficit/hyperactivity disorder (ADHD) and phthalate exposure, suggested the possible asso-ciation between phthalate metabolism and the inattention and hyperactive impulsivity phenotype of ADHD.

Food is the major source of several PAEs in humans and, particularly, of DEHP and DBP isomers,11 13 depending on environmental pollution and processing, storing, and packaging practices. Because DEHP and DBP are not chemically bound to plastic matrices, they can easily migrate, due to thermal or mechanic stress, into food contacting plastic surfaces and equipment such as containers, tubes, gloves, and packaging, including adhesives and imprints. The available data show that retail-packaged foods are widely contaminated by phthalate plasticizers2,12,14 17and that cooked foods, such as retail or hospital ready meals, can also be highly contaminated.18 This is why the EU has restricted phthalate use in food contact materials19and, to reduce the daily exposure to the more widely occurring phthalates, since 2005 the European Food Safety Authority (EFSA) has set tolerable daily intakes (TDIs) of 0.05 mg/kg body weight (bw) for DEHP and 0.01 mg/kg bw for DBP.20 22

Phthalate food contamination is considered to be of major im-portance, especially with regard to the age of consumers. Because Received: May 23, 2011

Revised: August 18, 2011 Accepted: September 6, 2011

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the toxicological profile of phthalates shows that developmental effects are the greatest concern, children have to be considered the most susceptible category. Because in the majority of indus-trialized countries, children attending school consume school meals, careful monitoring is required in terms of safety and, in this case, phthalate contamination.

This study aimed to evaluate children’s exposure to DEHP and DBP plasticizers from school meals and ascertain to what extent packaging can affect the concentration of such contaminants in ready-to-eat meals.

’ MATERIALS AND METHODS

Sampling.In Italy 3 10-year-old children make up the majority of refectory users. Generally, they have lunch at school, which is the main meal (40% of daily caloric contribution). According to local habits, a typical lunch is based on a first course of pasta or rice with tomato sauce or with legumes, vegetable soup, potato dumplings, etc.; a second course based on meat, fish, or dairy products; fresh or cooked vegetables; fresh fruit; and bread. The portions vary depending on the age of children (Table 1). The school meal service is supplied 5 or 6 days a week for about 8 10 months per year. In recent years, meals in Italian state schools have been mainly farmed out on contract to catering firms under the control of the Food Hygiene and Nutrition Service of the Italian Department of Health, which attempt with their nutritionists or dieticians to compile the diets to obtain well-balanced meals.

The production system consists mainly in food cooking, portioning quickly in disposable dishes that are sealed and transported up to 0.5 h away, maintaining the prescribed temperatures (>60°C or <4 10 °C) during transport. Thefirst courses are always cooked dishes, whereas the second courses may comprise cooked foods or foodstuffs not produced in the cateringfirms such as sliced cured meat (ham, salami) or dairy products (mozzarella, processed cheese) packed in plastic and served in their original industrial packaging. Bread consisted of rolls, also packed in sealed plastic by bakeries that deliver them to the cateringfirms on a daily basis.

To achieve our study aims, a cateringfirm supplying >1700 meals/day for nursery and primary schools in Naples (Italy) was involved. To evaluate the levels of DEHP and DBP and the influence of the packaging process in the meals supplied, the following were sampled from February to May 2010: (at the cateringfirm) foodstuffs before processing, in-cluding packed cured meats, dairy products, rolls, and fresh fruit, as well as cooked courses immediately before packaging; (at the schools supplied) packed ready meals at time of consumption.

In particular, almost 60 samples of foodstuffs, namely, cereals (pasta, rice), dry legumes (beans, lentils), potato dumplings, meat (fresh and cured), fish-based foods, dairy products (mozzarella cheese and processed cheese),

vegetables (frozen spinach, peas, carrots, chard; potatoes; canned maize), and condiments (olive oil, tomato sauce, onion, milk, eggs, Parmesan cheese, etc.), were collected twice (in February and April). As the menu changed every week (from Monday to Friday), meal sampling was car-ried out over a period of 4 weeks, with 20 complete meals being sampled before and after packaging. The meals consisted of afirst course, a second course, and vegetables (a total of 120 serving portions) plus bread (20 samples) and fruit (20 samples) (Table 1). The packaging in question consisted of polyethylene-coated aluminum (PE/Al) dishes thermally welded by polyethyleneterephthalate-coated aluminum (PET/Al) foil. The packed courses were placed on electrically powered isotherm serving carts, loaded onto vehicles, and delivered to schools. About 100 g of each food was put in glass jars that were hermetically closed by tops covered inside by an aluminum foil (rinsed twice with acetone and n-hexane) and transported to the laboratory, where the dry foods were ground and divided into 5 g aliquots; wet solid foods were homogenized, divided into 5 g aliquots, and lyophilized. As children consumed only peeled apples, pears, and oranges, the fresh fruit collected was peeled prior to being homogenized. Eggs were opened, and the content of each egg was weighed, homogenized, subdivided into 3 g aliquots, and lyoph-ilized. Liquids (olive oil and milk) were divided into 1 and 15 g aliquots, respectively; milk samples were lyophilized.

A complete portion of each ready course was collected immediately prior to packaging, put in a glass jar capped as described above, and taken to the laboratory, where it was codified, weighed, homogenized, subdivided into 5 g aliquots, and lyophilized. The packaged courses sampled at school were codified, weighed, homogenized, subdivided into 5 g aliquots, and lyophilized. All of the analytical samples were stored in airtight glass jars in the dark at 4°C until processed.

Chemicals.Acetonitrile, n-hexane, acetone for organic trace analysis, and anhydrous Na2SO4were supplied by Merck (Darmstadt, Germany). Florisil (60/100 mesh) was furnished by Supelco (Bellefonte, PA) and Bondesil (PSA 40UM) by Varian (Palo Alto, CA). Di(2-ethylhexyl)phthalate and dibutylphthalate standards were purchased from Sigma-Aldrich (Dorset, U.K.).

DEHP and DBP Detection.As the PAEs are ubiquitous, during each analytical phase several precautions were adopted to avoid con-tamination. All of the glassware used in sampling and in analytical activities was thoroughly washed and rinsed twice with acetone and n-hexane.

In accordance with the Tsumura et al.18 method, phthalates were extracted from food samples by 15 mL of acetonitrile three times in an ultrasound bath for 15 min; the samples were centrifuged at 2000 rpm for 10 min, transferring the acetonitrile layers to a separatory funnel; 10 mL of n-hexane saturated with acetonitrile was added, and the funnel was vigorously shaken for 5 min. The acetonitrile phase containing the phthalates was transferred to aflask and dried under vacuum at 55 °C. The dried extracts were reconstituted by 5 mL of n-hexane and cleaned Table 1. Composition and Mean Portion Sizes of School Meals Sampled

mean portion size (g)

meal component composition nursery school primary school

first course pasta or rice with tomato sauce and Parmesan cheese

or with legumes; pasta or rice in vegetable; vegetable soup; potato dumplings with minced meat; gateau

191 231

second course beef or pork stew or meatballs; frankfurters, ham;fish steaks; mozzarella or processed cheese

80 95

vegetables peas, potatoes, spinach with cheese, runner beans,

carrots, boiled chard dressed with olive oil, maize

80 108

fresh fruit apple, peer, orange 180 180

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up on a column consisting of 2 g of Florisil, activated for 2 h at 200°C, 0.5 g of Bondesil, and 1 g of anhydrous Na2SO4. The column was eluted three times with 10 mL of n-hexane/acetone (100:5 v/v), the eluates being collected. The eluates were evaporated under vacuum at 40°C and reconstituted with 2 mL of n-hexane for GC analysis. PAE analyses were carried out by a Shimadzu GC-17 (Shimadzu, Kyoto, Japan) capillary gas chromatograph with aflame ionization detector (FID), injecting 1 μL of each extract on an HP-5 (cross-linked 5% PHME Siloxane, 30 m length, 0.32 i.d., 0.25μm film thickness) glass capillary column. Helium was used as carrier and hydrogen/air for theflame. The injection mode was splitless, the injector temperature was 260°C, and the detector tem-perature was 310°C. The temperature program was 100 °C for 1 min, increasing by 15°C/min to 280 °C and staying at this temperature for 10 min.

Quantification and Quality Parameters. The calibration curves were made using DEHP and DBP standard solutions at three different levels, 2.50, 5.00, and 10.00μg/mL for DEHP and 1.25, 2.50, and 5.00μg/mL for DBP. Each concentration level was injected three times, and mean area value was considered to make the calibration curve. The regression coefficients (R) were >0.99 for both DEHP and DBP (Figures 1 and 2). The PAE concentrations (ng/g) were calculated by comparison with them.

To test the accuracy and validity of the method, the recoveries of DEHP and DBP from various spiked foods and meals were assessed. As PAE certified matrices are not available on the market, some represen-tative samples of different foodstuffs and serving portions were submit-ted to recovery tests, adding 1 mL of three standard solutions containing DEHP at 10.0, 20.0, and 40.0μg/mL and DBP at 5.0, 10.0, and 20.0 μg/mL and processing them as food samples. The recoveries obtained were 80.3( 3.5% for DEHP and 102.8( 4.4% for DBP.

To highlight possible contaminations a blank sample was tried with every series of analysis, and the value was subtracted from detected PAE values. Twenty blanks, obtained by submitting only the reagents to the analytical procedure, were analyzed, and LOD and LOQ values were obtained. For DEHP the LOD was 5.0 ng/g and the LOQ 15.0 ng/g, whereas for DBP the two values were 7.5 and 22.5 ng/g, respectively.

Statistical Analysis.To evaluate the influence of packaging on DEHP and DBP contamination levels, PAE contents in foods before and

after packaging were compared by log-transforming the values to ap-proximate a normal distribution of the data. All mean results are upper estimates that assume phthalates not detected as present at the limit of detection. Analysis of variance was carried out by ANOVA. The level of significance was set at p < 0.05. Statistical analysis was performed by SPSS 13.0.

’ RESULTS AND DISCUSSION

Figure 3 shows some GC chromatograms: one blank, two foodstuffs (raw pasta and cooked ham), and three courses after packaging (rice with tomato sauce, pork stew, and maize pan cooked).

The DEHP and DBP concentrations in foodstuffs are shown in Table 2. Among the foodstuffs are considered bread rolls and fruit results also, because these products were not processed and packaged in the catering industry. DEHP was found at detectable levels on average in 92% of foodstuffs analyzed and DBP in 76% of them. Meat,fish, and diary products, fresh fruit, and bread showed a 100% prevalence of DEHP contamination, followed by cereals and legumes (93%), vegetables (80%), and condiments (66%). Fish-based foods, fresh fruit, and bread showed a 100% prevalence of DBP contamination, followed by meat (85%), cereals and legumes (72%), dairy products (67%), vegetables (60%), and condiments (45%) (data not shown).

Bread andfish showed the highest DEHP concentrations, with median values, respectively, of 314.0 and 136.5 ng/g wet weight (ww). The highest DBP contents were found in bread rolls (101.0 ng/g ww), fresh fruit (66.0 ng/g ww), andfish (60.4 ng/g ww). The lowest concentrations of both DEHP and DBP were found in condiments (DEHP median concentration, 18.6 ng/g ww; range, 5.0 60.4 ng/g ww; DBP median, 7.5 ng/g ww; range, 7.5 19.2 ng/g ww). Except fresh fruit, the analyzed foods were less contaminated than cereals, bread, biscuits, cakes, nuts, spices, fat, and oil from Germany, the United Kingdom, and Japan (DEHP and DBP concentrations up to about 10 mg/kg) as reported by Wormuth et al.12

DEHP and DBP levels in cooked foods before and after pack-aging are respectively shown in Tables 3 and 4. Before packpack-aging, the DEHP median concentration levels varied from 111.4 to 154.8 ng/g ww; the lowest value was found among vegetables in a “spinach with cheese” dish (22.0 ng/g ww) and the highest among thefirst courses in “rice in vegetable soup” (379.4 ng/g ww).

In packaged meals sampled at schools the DEHP median values ranged from 127.0 to 253.3 ng/g ww; the lowest value was found again in“spinach with cheese” (21.3 ng/g ww) and the highest in afirst course of “rice with tomato sauce” (1050.8 ng/g ww) (Table 3).

The median concentrations of DBP before packaging ranged between 32.5 and 59.5 ng/g ww; the lowest value was found among vegetables in a sample of“boiled chard dressed with olive oil” (11.0 ng/g ww) and the highest among the first courses in “potato dumplings with minced meat” (165.4 ng/g ww). After packaging, the DBP median values ranged from 44.1 and 80.5 ng/g ww, with the lowest value (18.3 ng/g ww) among the second courses and in vegetables, respectively in“frankfurters” and “maize”; the most DBP-contaminated course was again“potato dumplings with minced meat” (775.0 ng/g ww) (Table 4). The DEHP and DBP median concentrations in cooked foods before packaging were lower than those after packaging at the time of consump-tion, with mean increases of 113% for DEHP and 125% for DBP and differences statistically significant between the first courses Figure 1. DEHP calibration curve in the range 2.50 10.00μg/mL.

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Table 2. DEHP and DBP Concentrations in Foodstuffs (n = 60), Fresh Fruit (n = 20), and Bread Rolls (n = 20) Sampled at the Catering Industry Involved in the Study

DEHP (ng/g ww) DBP (ng/g ww)

foodstuff mean( SD (min max) median mean( SD (min max) median

cereals and legumes 75.1( 87.8 (5.0 270.4) 38.4 50.5( 50.0 (7.5 152.4) 25.7

meat based 101.7( 88.4 (5.5 350.0) 80.0 52.2( 43.5 (7.5 147.0) 43.6 fish based 140.0( 52.2 (93.6 193.5) 136.5 81.1( 70.5 (23.8 180.0) 60.4 dairy 161.8( 235.5 (8.8 433.0) 43.6 32.2( 28.4 (7.5 63.2) 26.0 vegetables 87.2( 82.8 (5.0 265.2) 56.0 38.1( 46.2 (7.5 173.2) 20.2 condiments 22.8( 20.4 (5.0 60.4) 18.6 10.2( 4.0 (7.5 19.2) 7.5 fresh fruit 77.3( 34.9 (40.0 109.0) 83.0 57.0( 23.8 (30.0 75.0) 66.0 bread 270.3( 142.6 (111.0 386.0) 314.0 142.8( 78.0 (93.0 232.0) 101.0

Table 3. DEHP Concentrations in Ready Courses before (n = 60) and after Packaging at Consuming Time (n = 60)

DEHP (ng/g ww)

before packaging after packaging

course mean( SD (min max) median mean( SD (min max) median

firsta 146.6( 99.7 (37.9 379.4) 112.6 311.4( 255.1 (36.6 1050.8) 224.6

second 182.4( 100.3 (24.6 329.5) 154.8 250.4( 163.4 (43.6 497.2) 253.3

vegetables 117.0( 70.0 (22.6 365.0) 111.4 183.0( 140.4 (21.3 365.0) 127.0

aFirst course values showed statistically significant differences between before and after packaging (p = 0.02).

Figure 3. GC chromatograms of a blank (a), raw pasta (b), cooked ham (c), rice with tomato sauce after packaging (d), pork stew after packaging (e), and maize pan cooked after packaging (f).

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(for DEHP, p = 0.002; for DBP, p = 0.012). The total amount of DEHP and DBP for a meal, considering thefirst and second courses and the vegetables contributions, was calculated by multiplying the concentrations for the weight of each portion and summing the values obtained. Both DEHP and DBP contents showed a significant increase (p = 0.02) at time of consumption in comparison with the contents in unpacked courses (Table 5).

To estimate the school meal contribution to daily intake of DEHP and DBP in children, we determined the ratios of the total DEHP and DBP amounts per meal (first and second courses, vegetables, bread roll, and fruit) at time of consumption to children’s body weight. As suggested by the statistical reports of the Italian Society of Human Nutrition,23we considered for Italian children 3 5 years old (nursery school) a mean body weight (bw) of 17 kg and for those 6 10 years old (primary school) a mean body weight of 27 kg. We obtained a mean DEHP intake/meal of 8.6 ( 2.9 μg/kg bw (range, 4.2 17.7 μg/kg bw) in nursery school children and 6.3( 2.4 μg/kg bw (range, 2.8 12.9 μg/kg bw) in primary school children; the meal with highest intake levels consisted of rice with tomato sauce, ham and peas, bread roll, and apple. For DBP the mean intake/meal proved to be 5.4( 4.3 μg/kg bw (range, 2.4 16.9 μg/kg bw) in children 3 5 years old and 3.2( 2.1 μg/kg bw (range, 1.7 9.0 μg/kg bw) in those 6 10 years old (Table 6); the largest contributions to children’s daily intake were given by three meals comprising potato dumplings, pork stew and potatoes, bread roll, and apple; potato dumplings, processed cheese and peas, bread roll and apple; lentils with pasta, mozzarella cheese, and maize, bread roll, and apple (data not shown). In light of the TDI values (50μg/kg bw

for DEHP and 10μg/kg bw for DBP) established by the EFSA for adults of 70 kg bw,20we estimated on the basis of the mean and maximum values obtained that, in the study conditions, for nursery and primary school children DEHP intake via school meals can raise on average the respective TDI by 18% (maximum, 35%) and 12% (maximum, 26%) and DBP intake by 50% (maximum, 169%) and 30% (maximum, 90%). With regard to the maximum DBP contamination levels found in the meals at consumption, the intakes exceed the TDI in nursery school children and re-present 90% of the TDI in primary school pupils. If we were to calculate intakes by DBP mean concentrations obtained on meals before packaging, respectively 50.3μg in nursery school meals and 53.9μg in primary school meals, we would obtain much lower DBP intake levels/meal, never exceeding the TDI.

Various studies have estimated DEHP and DBP total daily intakes from food in adult populations (70 kg bw).13 28Mean total daily intakes for an adult of 70 kg bw varied from 2.1 to 4.9μg/kg bw for DEHP and from 0.2 to 4.2 μg/kg bw for DBP. For Danish children aged 1 6 and 7 14 years, M€uller et al.29 estimated mean TDIs, respectively, of 11.0 and 26.0μg/kg bw for DEHP and 3.5 and 8.0μg/kg bw for DBP. In the course of 1999 Tsumura et al. carried out two diverse studies on plasticizer contamination in meals served in three hospitals and in retail-packed lunches and set lunches from restaurants in Japan. They found DEHP contamination levels ranging from 10 to 4400 ng/g in composite meals from hospitals, estimating a mean intake of 519μg/day for hospitalized patients. Disposable PVC gloves used during the preparation of meals were suspected as the source of the high DEHP content.18In the retail packed lunches analyzed, the levels of DEHP were much higher (346 11800 ng/g), where-as set lunches from restaurants were much less contaminated (12 304 ng/g). Disposable PVC gloves, sprayed with 68% ethanol to sterilize them, used in the factories producing the packed lunches, were confirmed as the principal source of DEHP contamination.30A further study carried out in 2001 by the same authors, following the regulation of DEHP-containing PVC gloves in Japan, showed that the DEHP levels in the hospital meals were Table 4. DBP Concentrations in Ready Courses before (n = 60) and after Packaging at Consuming Time (n = 60)

DBP (ng/g ww)

before packaging after packaging

course mean( SD (min max) median mean( SD (min max) median

firsta 65.4( 40.6 (16.4 165.4) 59.5 169.3( 217.7 (19.9 775.0) 80.5

second 51.9( 35.5 (19.8 112.5) 33.1 86.8( 93.4 (18.3 336.8) 44.1

vegetables 42.1( 27.4 (11.0 91.0) 32.5 92.9( 82.5 (18.3 236.1) 68.8

aFirst course values showed statistically significant differences between before and after packaging (p = 0.012). Table 5. DEHP and DBP Contents in Nursery and Primary School Meals before and after Packaging

PAEs (mean( SD (range), μg)

nursery school primary school

PAE before packaging after packaging before packaging after packaging

DEHP 101.9( 22.9 (69.0 152.0) 144.9( 48.8 (72.0 301.0) 125.3( 40.6 (71.0 228.0) 170.0( 63.9 (76.0 348.0)

DBP 50.3( 11.5 (36.4 79.4) 91.2( 71.6 (41.4 272.8) 53.9( 11.0 (38.4 81.5) 86.8( 57.3 (45.4 243.4)

Table 6. DEHP and DBP Intake by School Meal for Children of Nursery and Primary Schools

intake (mean( SD (min max), μg/kg bw/meal)

PAE nursery school primary school

DEHP 8.6( 2.9 (4.2 17.7) 6.3( 2.4 (2.8 12.9)

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much lower (6 675 ng/g) ,and hence the estimated DEHP mean daily intake decreased to 160μg.31

In conclusion, foodstuffs used to prepare meals analyzed in the present study showed diffuse contamination by DEHP and DBP, confirming the ubiquity of the contamination sources. The highest concentrations of DEHP and DBP were found mainly in the processed and packed foodstuffs employed in supplying school meals, suggesting that manufacturing and contact with plastic wrapping can play a major role in the phthalate contam-ination of foods, as shown also by the high levels of DEHP and DBP found in bread rolls that are quickly packed after baking at a temperature that can favor plasticizer release. The increase in DEHP and DBP concentrations in the courses after packaging testified to the influence of the contact of cooked foods with the kind of packaging (PE/Al dishes thermally welded by PET/Al foil) used in the cateringfirm considered. Among the various courses comprising the meal, thefirst courses showed the highest concentrations, with a significant (p = 0.02) increase of both DEHP and DBP after packaging. Those that, as described above, were based on pasta or rice with tomato sauce or legumes, vegetable soup, etc., and various condiments are the courses with the more complex composition that can maintain a high tempera-ture (>60°C) for a time longer than the other courses. Further-more, their weight and volume are much higher than those of the other courses, so thefirst courses may establish maximum con-tact with package surfaces. The presence of tomato sauce or other liquid fat condiments (olive oil, milk, cream, etc.) could further influence the release of the package plasticizers. It may also be considered that after cooking, foods are quickly portioned and packed to be transported (up to 0.5 h) and served to children, but, as observed during the collection of the meals at the served schools, the time of transport can noticeably vary up to 1 2 h depending on traffic.

The DEHP and DBP intake values estimated in the present study are noticeably variable and, even if referred only to the lunch, can reach levels near or up to the TDI. School meals supplied in the described conditions could be improved to increase the safety of foods, reducing the phthalate contamination levels. Even if in the present study the influence of the temperature and time of contact or the specific composition of the courses, for example, the lipidic content, has not been studied, it is plausible that these parameters could influence the migration of the plasticizers from the packages into the foods. The reduction of the times between the cooking and serving of the meals and/or the choice of an alternative packaging could be good options to reduce precau-tionally the risks for the children’s health.

’ AUTHOR INFORMATION Corresponding Author

*Phone: +39 081 2539450. Fax: +39 081 2539407. E-mail: tcirillo@unina.it.

’ REFERENCES

(1) Landrigan, P.; Garg, A.; Droller, D. B. J. Assessing the effects of endocrine disruptors in the National Children’s Study. Environ. Health Perspect. 2003, 111, 1678–1681.

(2) Sheela, S. Phthalates and children’s health. Curr. Probl. Pediatr. Adol. Health Care 2008, 38, 34–49.

(3) ATSDR (Agency for Toxic Substances and Disease Registry). Toxicological Profile for Di-n-butyl Phthalate; U.S. Department of Health and Human Services, Public Health Service, Agency for Toxic Sub-stances and Disease Registry: Atlanta, GA, 2001.

(4) ATSDR (Agency for Toxic Substances and Disease Registry). Toxicological Profile for Di(2-ethylhexyl)phthalate (DEHP); U.S. Depart-ment of Health and Human Services, Public Health Service, Agency for Toxic Substances and Disease Registry: Atlanta, GA, 2002.

(5) Moore, R. W.; Rudy, T. A.; Lin, T. M.; Ko, K. Abnormalities of sexual development in male rats with in utero and lactational exposure to the antiandrogenic plasticizer di(2-ethylhexyl)phthalate. Environ. Health Perspect. 2001, 109, 229–237.

(6) Fisher, J. S.; Macpherson, S.; Marchetti, N.; Sharpe, R. M. Human “testicular dysgenesis syndrome”: a possible model using in-utero exposure of the rat to dibutyl phthalate. Hum. Reprod. 2003, 18, 1383–1394.

(7) Skakkebæk, N. E.; Jørgensen, N.; Main, K. M.; Rajpert-De Meyts, E. Is human fecundity declining? Int. J. Androl. 2006, 29, 2–11.

(8) Hauser, R.; Calafat, A. M. Phthalates and human health. Occup. Environ. Med. 2005, 62, 806–818.

(9) ECB (European Chemicals Bureau). Dibutyl phthalate Risk Assessment; Report Special Publication I.01.66; Institute for Health and Consumer Protection: Ispra, Italy, 2004; http://ecb.jrc.it.

(10) Kim, B. N.; Cho, S. C.; Kim, Y.; Shin, M. S.; Yoo, H. J.; Kim, J. W.; Yang, Y. H.; Kim, H. W.; Bhang, S. Y.; Hong, Y. C. Phthalates exposure and attention-deficit/hyperactivity disorder in school-age children. Biol. Psychiatry 2009, 66, 958–963.

(11) Latini, G.; De Felice, C.; Presta, G.; Del Vecchio, A.; Paris, I.; Ruggieri, F. In utero exposure to di-(2-ethylhexyl) phthalate and duration of human pregnancy. Environ. Health Perspect. 2003, 111, 1783–1785.

(12) Wormuth, M.; Scheringer, M.; Vollenweider, M.; Hungerbuhler, K. What are the sources of exposure to eight frequently used phthalic acid esters in Europeans? Risk Anal. 2006, 26, 803–824.

(13) Fromme, H.; Gruber, L.; Schlummer, M.; Wolz, G.; Bohmer, S.; Angerer, J. Intake of phthalates and di(2-ethylhexyl) adipate: results of the Integrated Exposure Assessment Survey based on duplicate diet samples and biomonitoring data. Environ. Int. 2007, 33, 1012–1020.

(14) Castle, L.; Mercer, A. J.; Startin, J. R.; Gilbert, J. Migration from plasticizedfilms into foods. 3. Migration of phthalate, sebacate, citrate and phosphate-esters fromfilms used for retail food packaging. Food Add Contam. 1988, 5, 9–20.

(15) Kueseng, P.; Thavarungkul, P.; Kanatharana, P. Trace phthalate and adipate esters contaminated in packaged food. J. Environ. Sci. Health B 2007, 42, 569–576.

(16) Lhuguenot, J. C. L. Recent European Food Safety Authority toxicological evaluations of major phthalates used in food contact materials. Mol. Nutr. Food Res. 2009, 53, 1063–1070.

(17) Spillmann, M. D.; Siegrist, M.; Keller, C.; Wormuth, M. Phthalate exposure through food and consumers’ risk perception of chemicals in food. Risk Anal. 2009, 29, 1170–1180.

(18) Tsumura, Y.; Ishimitsu, S.; Saito, H.; Kobayashi, Y.; Tonogai, Y. Eleven phthalate esters and di(2-ethylhexyl) adipate in one-week duplicate diet samples obtained from hospitals and their estimated daily intake. Food Addit. Contam. 2001, 18, 449–460.

(19) Regulation (EC) No 1935/2004 of the European Parliament and of the Council. On materials and articles intended to come into contact with food and repealing Directives 80/590/EEC and 89/109/ EEC. Off. J. Eur. Union 2004, L338/4 13.11.2004.

(20) EFSA (European Food Safety Authority). Statement of the Scientific Panel on Food Additives, Flavourings, Processing Aids and Material in Contact with Food (AFC) on a request from the Commis-sion on the possibility of allocating a group-TDI for butylbenzylphtha-late (BBP), dibutylphthabutylbenzylphtha-late (DBP), bis(2-ethylhexyl)phthabutylbenzylphtha-late (DEHP), di-isononylphthalate (DINP) and di-isodecylphthalate (DIDP). Minute expressed at 12thPlenary meeting on June 28, 2005.

(21) EFSA (European Food Safety Authority). Di-butylphthalate (DBP) for use in food contact materials. Opinion of the Scientific Panel on Food Additives, Flavourings; Processing Aids and Material in Contact with Food (AFC). EFSA J. 2005, 242, 1 17.

(22) EFSA (European Food Safety Authority). Opinion of the Scientific Panel on Food Additives, Flavourings, Processing Aids and Materials in Contact with Food (AFC) on a request from the Commis-sion related to Bis(2-ethylhexyl)phthalate (DEHP) for use in food

(7)

contact materials Question No. EFSA-Q-2003-191. EFSA J. 2005, 243, 1 20.

(23) SINU (Societa Italiana di Nutrizione Umana). Livelli di Assun-zione Raccomandati di Energia e Nutrienti; Istituto Nazionale della Nutrizione. Rome, Italy, 1996.

(24) Pfannhauser, W.; Leitner, E.; Siegl, H. Phthalate. In Lebensmit-teln. Forschungsbericht Sektion III; €Osterreichisches Bundesministerium f€ur Gesundheit und Konsumentenschutz: Wien, Austria, 1995.

(25) MAFF Ministry of Agriculture, Fisheries and Food. Survey of Plasticiser Levels in Food Contact Materials and in Foods; Food Surveillance Papers 21; 1996.

(26) Petersen, J. H.; Breindahl, T. Plasticizers in total diet samples, baby food and infant formulae. Food Addit. Contam. 2000, 17, 133–141. (27) DEHRM (Division of Environmental Health & Risk Manage-ment), University of Birmingham. Measuring the Bioavailability of Human Dietary Intake of PAH; Phthalates and Aromatic Hydrocarbons; report prepared for the Food Standards Agency; London, U.K., 2003.

(28) Colacino, J. A.; Harris, T. R.; Schecter, A. Dietary Intake is associated with phthalate body burden in a nationally representative sample. Environ. Health Perspect. 2010, 118, 998–1003.

(29) M€uller, A. M.; Nielsen, A.; Ladefoged, O. Ministeriet for Fødevarer, Landbrug og Fiskeri Veterinær- og Fødevare direktoratet rapport. Human Exposure to Selected Phthalates in Denmark; 2003.

(30) Tsumura, Y.; Ishimitsu, S.; Kaihara, A.; Yoshii, K.; Nakamura, Y.; Tonogai, Y. Di(2-ethylhexyl) phthalate contamination of retail packed lunches caused by PVC gloves used in the preparation of foods. Food Addit. Contam. 2001, 18, 569–579.

(31) Tsumura, Y.; Ishimitsu, S.; Saito, I.; Sakai, H.; Tsuchida, Y.; Tonogai, Y. Estimated daily intake of plasticizers in 1-week duplicate diet samples following regulation of DEHP-containing PVC gloves in Japan. Food Addit. Contam. 2003, 20, 317–324.

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